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系统性红斑狼疮的磷脂酶C-γ的致病机制及靶向治疗研究进展

Research progress on the phospholipase C-gamma pathogenesis mechanism of systemic lupus erythematotus (SLE) and its targeting therapy
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摘要 磷脂酶C(PLC)是磷脂酰肌醇信号通路的关键酶。磷脂酰肌醇4,5二磷酸(PIP2)在活化的PLC作用下水解为二酯酰甘油(DAG)和肌醇三磷酸(IP3),这两种第二信使传递细胞外信息给下游效应分子,调节细胞的生命活动。PLC-γ是PLC的一种亚型,主要由蛋白酪氨酸激酶(PTK)激活,包括PLC-γ1与PLC-γ2两个亚型。系统性红斑狼疮(SLE)以对核抗原耐受性缺陷为特征,这与T、B细胞受体信号转导异常有关。SLE中PLC-γ1、γ2表达均增强。酪氨酸激酶在免疫细胞信号通路中起关键作用,现就PLC-γ的生物学功能、活化方式及其在红斑狼疮中的免疫机制以及SLE靶向治疗研究做一综述。 Phospholipase C(PLC) is a key enzyme in signal pathway of phosploa tidylinositol receptors for extracellular stimuli promote activation of PLC,which converts phosphatidylinositol (4,5) bisphosphate (PtdIns (4,5) P2) into the Ca2+-mobilizing second messenger,inositol (1,4,5) trisphosphate (Ins (1,4,5)P3),and the protein kinase-activating second messenger,diacylglycerol (DAG). Two PLC-γ isozymes (PLC-γ1 and PLC-γ2) exist in mammals. PLC-γ isozymes are activated by a panoply of growth factors and immunological stimuli that signal throughreceptor and non-receptor tyrosine kinases. Among the cells in the immune system,the B cells and T cell in SLE patients have multiple abnormalities that may account for the ongoing autoantibody production and the initiation and maintenance of the autoimmune reaction. Tyrosine kinases play a central role in signaling processes in the cells known to be important in the pathogenesis of autoimmune diseases. In this article authors summarize the function of tyrosine kinases and their novel inhibitors as therapeutic targets from studies made in animal lupus models and systemic lupus erythematosus patients.
作者 孟凡华 葛彦明 王素霞 刘长瑞 MENG Fan-ha,GE Yan-ming,WANG Su-qin,et al( Dept. of Blood Purification,the General Hospital of Jinan Military Region,Jinan,Shandong 250031 ,China)
出处 《实用医药杂志》 2017年第3期269-271,共3页 Practical Journal of Medicine & Pharmacy
关键词 磷脂酶PLC-γ 生物学功能 活化 系统性红斑狼疮 酪氨酸激酶抑制药 靶向治疗 Phospholipase C-gamma(PLC-γ) Biological function Activation Systemic lupus erythematosus (SLE) Inhibitor of tyrosine kinases Targeting treatment
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